Search results for "Metabolic acidosis"

showing 10 items of 17 documents

Thiamine for the treatment of nucleoside analogue-induced severe lactic acidosis

1999

Nucleoside analogue-induced lactic acidosis is an often fatal condition in patients with HIV. There is only one report of successful treatment with riboflavin. We describe a 30-year-old female with AIDS and nucleoside analogue-induced lactic acidosis that exacerbated shortly after introducing total parenteral nutrition and reversed within hours after the addition of thiamine. Successful treatment of nucleoside analogue-induced lactic acidosis with a high dose of thiamine supports the hypothesis that vitamin deficiency is an important cofactor in the development of this rare and unpredictable condition in patients with HIV. We suggest that high dose B-vitamins should be given to any patient …

AdultAnti-HIV AgentsPharmacologymedicineHumansThiamineAcidosisAcquired Immunodeficiency SyndromeNucleoside analoguebusiness.industryfood and beveragesMetabolic acidosismedicine.diseaseDidanosineStavudineB vitaminsAnesthesiology and Pain MedicineBiochemistryLactic acidosisAcidosis LacticFemaleParenteral Nutrition TotalThiaminemedicine.symptombusinessSevere lactic acidosisNucleosidemedicine.drugEuropean Journal of Anaesthesiology
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Whole-body potassium and bone mineral density up to 30 years after urinary diversion

1998

Objectives  To evaluate the long-term effects of different types of urinary diversion on skeletal bone density and whole-body potassium content in patients with an early correction of base excess (<−2.5). Patients and methods  The early correction of base excess (<−2.5) is one of the principles of the treatment of patients undergoing urinary diversion at our institution. In 27 patients with urinary diversion, bone mineral density (assessed by dual-photon absorptiometry), whole-body potassium, electrolyte and creatinine levels were determined, and capillary blood gas analysed. The mean time since surgery was 16.8 years in 16 patients with a rectal reservoir, 20.5 years in six patients with a…

AdultMalemedicine.medical_specialtyTime FactorsAdolescentBone densityUrologymedicine.medical_treatmentUrologyUrineUrinary Diversionchemistry.chemical_compoundMetabolic DiseasesBone DensitymedicineHumansChildAgedBone mineralCreatininebusiness.industryUrinary diversionMetabolic acidosisMiddle Agedmedicine.diseaseSurgerychemistryPotassiumFemaleBase excessPouchbusinessFollow-Up StudiesBJU International
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The diabetic ketoacidosis

2014

The Diabetic Ketoacidosis (DKA) is still today a medical emergency in pediatrics. Despite the latest great sensibilization of the population and the doctors, the risk of DKA has not yet been eliminated and this pathology is still occurring in 25 to 40% of diabetes onset cases, in already diagnosed patients with poor compliance (10%), in patients undergoing acute medical or surgical events or in patients in Continuous Subcoutaneous Insulin Therapy (CSII). In toddlers (0-3 years) it is twice more frequent than in the following ages and is characterized by the presence of more serious clinical dehydratation (>10%) and neurological signs (obnubilation 40%). The other category at risk is represe…

Body surface areaeducation.field_of_studyPediatricsmedicine.medical_specialtyDiabetic ketoacidosisbusiness.industryInsulinmedicine.medical_treatmentPopulationMetabolic acidosismedicine.diseaseDiabetes mellitusMeeting AbstractmedicineRegular insulineducationComplicationbusinessItalian Journal of Pediatrics
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Clinical manifestations and management of four children with Pearson syndrome.

2011

Pearson marrow-pancreas syndrome is a fatal disorder mostly diagnosed during infancy and caused by mutations of mitochondrial DNA. We hereby report on four children affected by Pearson syndrome with hematological disorders at onset. The disease was fatal to three of them and the fourth one, who received hematopoietic stem cell transplantation, died of secondary malignancy. In this latter patient transplantation corrected hematological and non-hematological issues like metabolic acidosis, and we therefore argue that it could be considered as a useful option in an early stage of the disease.

MalePediatricsmedicine.medical_specialtyMitochondrial DiseasesAnemiaMitochondrial diseasemedicine.medical_treatmenttrapianto cellule staminali emopoieticheHematopoietic stem cell transplantationDiseaseDNA MitochondrialLipid Metabolism Inborn Errorsmitochondrial disordersFatal OutcomeMuscular DiseasesCause of Deathhematopoietic stem cell transplantation; mitochondrial disorders; Pearson marrow-pancreas syndrome; trapianto cellule staminali emopoietiche; malattie mitocondriali; sindrome di PearsonGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansChildGenetics (clinical)Pearson marrow-pancreas syndromeCause of deathPearson syndromebusiness.industryAcyl-CoA Dehydrogenase Long-ChainHematopoietic Stem Cell TransplantationInfantMetabolic acidosissindrome di Pearsonmedicine.diseaseAnemia SideroblasticTransplantationChild PreschoolImmunologymalattie mitocondrialiFemalebusinessGene DeletionAmerican journal of medical genetics. Part A
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Mitochondrial myopathy with lactic acidosis and deficient activity of muscle succinate cytochrome-c-oxidoreductase

1984

A male infant had severe muscular hypotonia from birth. Recurrent vomiting with dehydration and severe metabolic acidosis complicated the course. Elevated lactate (up to 12.3 mmol/l; n less than 2), pyruvate (0.4 mmol/l; n less than 0.05) and alanine levels were found in serum with an abnormal lactate/pyruvate ratio (greater than 30; n less than 15). In urine the concentrations of lactate, pyruvate, alanine and of several intermediates of the citric acid cycle were increased. In muscle, numerous disseminated "ragged red fibres" were found by light microscopy; muscle fibres were found to contain subsarcolemmal aggregates of mitochondria, lipid droplets and glycogen by electromicroscopical me…

Malemedicine.medical_specialtySevere muscular hypotoniaRespiratory chainMitochondria Livermacromolecular substancesMitochondrionBiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineMuscular DiseasesMitochondrial myopathy030225 pediatricsInternal medicinemedicineHumansGlycogenMusclesInfantMetabolic acidosismedicine.diseaseMitochondriaMitochondria Muscle3. Good healthCitric acid cycleEndocrinologyBiochemistrychemistryLactic acidosisPediatrics Perinatology and Child HealthLactatesSuccinate Cytochrome c OxidoreductaseAcidosisOxidoreductases030217 neurology & neurosurgeryEuropean Journal of Pediatrics
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C1-ESTERASE INHIBITOR REVERSES FUNCTIONAL CONSEQUENCES OF SUPERIOR MESENTERIC ARTERY ISCHEMIA/REPERFUSION BY LIMITING REPERFUSION INJURY AND RESTORIN…

2006

Activated complement contributes significantly to reperfusion injury after ischemia. This study explores functional consequences of C1-esterase inhibitor (C1-INH) treatment after superior mesenteric artery occlusion (SMAO)/ reperfusion using intravital microscopy. Thirty anesthetized, spontaneously breathing, male Sprague-Dawley rats underwent SMAO for 60 min followed by reperfusion (4 h). C1-esterase inhibitor (100 and 200 IU/kg body weight) or saline (0.9%) was given as a single bolus before reperfusion. Sham-operated animals (n = 10) without SMAO served as controls.Systemichemodynamicsweremonitoredcontinuously,arterial bloodgasesanalyzedintermittently, andleukocyte/ endothelial interacti…

Malemedicine.medical_treatmentIschemiaPharmacologyCritical Care and Intensive Care MedicineRats Sprague-DawleyBolus (medicine)Mesenteric Artery Superiormedicine.arterymedicineAnimalsSuperior mesenteric arterySalinebusiness.industryMicrocirculationMetabolic acidosismedicine.diseaseRatsRegional Blood FlowMesenteric ischemiaReperfusion InjuryAnesthesiaEmergency MedicinebusinessComplement C1 Inhibitor ProteinReperfusion injuryIntravital microscopyShock
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DEFECTIVE JEJUNAL BRUSH BORDER Na+/H+ EXCHANGE IN LETHAL FAMILIAN PROTRACTED DIARRHOEA

1989

The clinical spectrum of disease associated with the recently described defect in jejunal brush border membrane (BBM) Na+/H+ exchange remains poorly defined. We describe a further, lethal case of protracted diarrhoea in a child from a family in whom 2 previous siblings died of protracted diarrhoea at 2 and 11 months. The patient, a boy, was born at term weighing 2.9 kg and was admitted at 6d with profuse watery diarrhoea, severe dehydration and metabolic acidosis. Parenteral nutrition was started but the diarrhoea persisted, and he developed severe necrotising enterocolitis requiring an ileostomy. A high-output secretory diarrhoea persisted during nil by mouth (ileostomy fluid mmol/l: Na+ 1…

Pathologymedicine.medical_specialtyBrush borderbusiness.industryGlucose uptakemedicine.medical_treatmentMetabolic acidosismedicine.diseaseGastroenterologyIleostomyParenteral nutritionInternal medicinePediatrics Perinatology and Child HealthmedicineJejunal biopsyProtracted diarrhoeabusinessGastrointestinal functionPediatric Research
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Die renale S�ure- und Ammonium-Ionen-Ausscheidung normaler und adrenalektomierter Ratten und ihre Beeinflussung durch Nebennierenrindenhormone

1959

The renal excretion of acid and ammonium ions after an oral load of monosodium-phosphate (1.2 mEq. per rat) was studied in groups of adrenalectomized er sham-operated rats, maintained on 0.9 per cent NaCI solution and water, on the 6th or 12th day after operation. Untreated groups were compared to groups receiving either Corticotropin (25 U./kg./day s.c.) or Cortisone acetate (12.5 mg./kg./day s.c.) er (7.5 mg./kg./day s.c.) or D,L-Aldosterone acetate Cortexone acetate (0.15 mg./kg./day s.c.) from the 3rd to the 12th day after opetarion. In sham-operated rats Cortisone increased H+ excretion and diuresis on the 6th day after operation (3rd day of treatment). This influence did not persist o…

Pharmacologymedicine.medical_specialtyAldosteroneChemistryDiuresisMetabolic acidosisGeneral Medicinemedicine.diseaseExcretionchemistry.chemical_compoundEndocrinologyRenal physiologyInternal medicinemedicineAmmoniumCortisonemedicine.drugHormoneNaunyn-Schmiedebergs Archiv f�r Experimentelle Pathologie und Pharmakologie
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pH-dependent hydrolysis of acetylcholine: Consequences for non-neuronal acetylcholine

2015

Acetylcholine is inactivated by acetylcholinesterase and butyrylcholinesterase and thereby its cellular signalling is stopped. One distinguishing difference between the neuronal and non-neuronal cholinergic system is the high expression level of the esterase activity within the former and a considerably lower level within the latter system. Thus, any situation which limits the activity of both esterases will affect the non-neuronal cholinergic system to a much greater extent than the neuronal one. Both esterases are pH-dependent with an optimum at pH above 7, whereas at pH values below 6 particularly the specific acetylcholinesterase is more or less inactive. Thus, acetylcholine is prevente…

Pharmacologymedicine.medical_specialtyHydrolysisImmunologyMetabolic acidosisHydrogen-Ion Concentrationmedicine.diseaseAcetylcholinesteraseEsteraseAcetylcholinechemistry.chemical_compoundEndocrinologychemistryButyrylcholinesteraseInternal medicineAcetylcholinesterasemedicineExtracellularHumansImmunology and AllergyCholinergicAcetylcholineButyrylcholinesterasemedicine.drugCalcium signalingInternational Immunopharmacology
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Alteration of anion gap during almost total plasma replacement with synthetic colloids in piglets

2000

In ten piglets (body weight 8.2-11.6 kg), acid base, electrolyte and anion gap changes were investigated during almost total plasma replacement with hydroxyethyl starch (HES) and modified fluid gelatin (GEL) in saline solution using a cell saver autotransfusion technique. During the study, there were only moderate acid base changes, but marked disturbances in anion balance. At study end, the mean chloride concentration was significantly higher (mmol/l: normal values 97-108, HES 116 +/- 1.5, GEL 108 +/- 1.1, p0.01) and the mean anion gap was significantly lower in the HES group in comparison to the GEL group (mmol/l: normal values 5-14, HES 3 +/- 1.7, GEL 11.9 +/- 0.9, p0.01). It is conclude…

Swinemedicine.medical_treatmentPlasma SubstitutesAnion gapAcid–base homeostasisElectrolyteHydroxyethyl starchCritical Care and Intensive Care MedicineChlorideHydroxyethyl Starch DerivativesBlood Transfusion AutologousElectrolytesRandom AllocationColloidmedicineAnimalsColloidsSalineAcid-Base EquilibriumChromatographybusiness.industrySuccinatesMetabolic acidosisHydrogen-Ion Concentrationmedicine.diseaseDisease Models AnimalAnimals NewbornBiochemistryFluid TherapyGelatinFemalebusinessmedicine.drugIntensive Care Medicine
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